Deficits in sensory gating are believed to be involved in a variety of clinical symptoms and disrupted cognitive functions in patients with schizophrenia. The psychological and biological mechanisms of normal and impaired gating, and why some novel antipsychotic medications improve gating while conventional antipsychotics do not, are not well understood. Progress toward understanding neural mechanisms involved in gating can contribute to theory about schizophrenia and to its treatment. A prominent research paradigm for studying gating deficits in schizophrenia involves presentation of a pair of clicks and noninvasive measurement of the P50 component of the associated event-related brain potential. P50 amplitude to the second click is normally reduced substantially from that to the first click, but patients (and some of their family members) commonly show less reduction, i.e. have impaired gating. The proposed project will address three pressing issues surrounding this well-established finding. (1) What are the neural generators of P50? Are they confined to bilateral superior temporal gyrus? (2) How are those generators affected by antipsychotic medication, is the effect equal across the generators, and is the effect different for conventional vs. novel antipsychotics? (3) Is the gating deficit specific to auditory stimuli, or is it cross modal as the literature assumes? This application presents extensive pilot data addressing all three of these issues in hopes of furthering our understanding of impaired sensory gating in schizophrenia.